Kainate-receptor-mediated sensory synaptic transmission in mammalian spinal cord

Ping Li, Timothy J. Wilding, Susan J. Kim, Amelita A. Calejesan, James E. Huettner and Min Zhuo ()
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Ping Li: Departments of Anesthesiology
Timothy J. Wilding: Departments of Cell Biology and Physiology
Susan J. Kim: Departments of Anesthesiology
Amelita A. Calejesan: Departments of Anesthesiology
James E. Huettner: Departments of Cell Biology and Physiology
Min Zhuo: Departments of Anesthesiology

Nature, 1999, vol. 397, issue 6715, 161-164

Abstract: Abstract Glutamate, the major excitatory neurotransmitter in the central nervous system, activates three different receptors that directly gate ion channels, namely receptors for AMPA (α-amino-3-hydroxy-5-methyl isoxozole propionic acid), NMDA (N-methyl-D-aspartate), and kainate, a structural analogue of glutamate. The contribution of AMPA and NMDA receptors to synaptic transmission and plasticity is well established1. Recent work on the physiological function of kainate receptors has focused on the hippocampus2, where repetitive activation of the mossy-fibre pathway generates a slow, kainate-receptor-mediated excitatory postsynaptic current (EPSC)3,4,5. Here we show that high-intensity single-shock stimulation (of duration 200 microseconds) of primary afferent sensory fibres produces a fast, kainate-receptor-mediated EPSC in the superficial dorsal horn of the spinal cord. Activation of low-threshold afferent fibres generates typical AMPA-receptor-mediated EPSCs only, indicating that kainate receptors may be restricted to synapses formed by high-threshold nociceptive (pain-sensing) and thermoreceptive primary afferent fibres. Consistent with this possibility, kainate-receptor-mediated EPSCs are blocked by the analgesic µ-opiate-receptor agonist Damgo and spinal blockade of both kainate and AMPA receptors produces antinociception. Thus, spinal kainate receptors contribute to transmission of somatosensory inputs from the periphery to the brain.

Date: 1999
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DOI: 10.1038/16469

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